This project investigates the behavioral and physiological changes that occur in the processing of persistent noxious input associated with inflammation. The specific aims of this project were to: (1) determine how persistent inflammation alters the monkey's ability to detect innocuous and noxious thermal stimulation, (2) examine the changes that occur in the primary somatosensory cortex during persistent inflammation (3) explore the role of NMDA receptor activity in the changes that result from persistent inflammation. The influence of inflammation on the monkey's ability to detect thermal stimulation was examined. A day after subcutaneous injections of carrageenan, the monkey's hand increased approximately 65% in volume. The monkey's detection speed to innocuous and noxious thermal stimuli increased dramatically for the next two days and then returned to near normal over the next week. These data suggest that the period of hyperalgesia produced by the inflammation was followed by a period of allodynia. The neuronal mechanisms subserving the hyperalgesia and allodynia that result from inflammation were investigated in the primary somatosensory cortex of the anesthetized monkey. Wide-dynamic-range neurons, which are responsive to innocuous mechanical stimuli but the maximum response was to noxious mechanical stimuli, were isolated 24 hours after inflammation. Compared to control, inflammation did not change receptive size of the wide-dynamic-range nociceptive neurons, the spontaneous activity or response to mechanical or thermal stimulation. The data from these studies suggest that these neurons are not involved in the processing of persistent painful input such as that caused by inflammation. In the present study a limited number of nociceptive specific neurons, responsive to only noxious mechanical stimulation, were encountered. The response properties of these neurons make them likely candidates to subserve the allodynia and hyperalgesia that accompanies inflammation.